Identity and topographic localization of immunocompetent cells and alteration of surface markers on ocular resident cells in rodents with experimental autoimmune uveoretinitis by active immunization or adoptive transfer were analyzed by immunohistochemical studies. The lymphocyte population at the inflammatory sites was found to change markedly during the course of disease. In the early stage, T-helper/inducers are the predominant cells in the eye. A relative increase of T-suppressor/cytotoxic cells in the late stage were observed. Expression of major histocompatibility complex class II antigens on ocular resident cells such as RPE, retinal endothelium, keratocytes, fibroblast and ciliary epithelium was observed in different models of EAU in rats. This antigen expression may play a certain role in the pathogenesis of EAU. Both infiltrating (cell subpopulation) and expression of class II antigens on ocular resident cells, can be modulated by different immunosuppressive agents. Dynamics of EAU induced by adoptive transfer of S-antigen-specific T-lymphocyte cell line has showed that this cell line can recognize the photoreceptor S-Ag in vivo. Immunopathology in the eyes with EAU in mice can be presented as a chronic granulomatous inflammation. Development of subretinal neovascularization may occur. Expression of major histocompatibility complex class II antigens is only located on ocular resident cells with the presence of inflammatory cells.